The Receptor of Activated C Kinase (RACK-1) has been previously shown as an interactor of miRISC in C. elegant and human. It was proposed that RACK-1 contributes to the recruitment of miRISC to the active ribosomes and repression of RACK-1 may impair miRNA function. In C. elegans, the let-7 miRNA regulates the exit of cell cycle and terminal differentiation. Dysfunction of let-7 results in irregular hypodermal and vulval development. Here we examined the effects of repression of RACK-1 on let-7 function using the wild-type let-7 allele and a ts mutant let-7 allele that expresses a lower amount of let-7. Indeed, in wild-type worms we observed a small fraction of animals showing let-7 defect phenotypes, as shown in the previous studies. However, interestingly, we found that repression of RACK-1 significantly suppressed the defect phenotypes of the ts let-7(n2853) allele. Moreover, repression of RACK-1 resulted in increased levels of let-7 in both wild-type or let-7(n2853) mutant worms. Our results suggest that beside contributing to the recruitment of miRISC, RACK-1 alters the let-7 level via an unknown mechanism. *corresponding authors